HAEMORRHAGE
CONTENTS
. Introduction
. Definition
. Classification
. Causes Of Haemorrhage
. Clinical Features
. Hematological Features
. Haemostasis
. Stages Of Haemostasis
. Methods Of Achieving Haemostasis
. Wound Healing
. Healing Of Extraction Socket
. Complications
. Recent Advances
. Conclusion
. Reference
INTRODUCTION
• Haemorrhage can occur a greater or lesser degree during all surgical
procedures. Major hemorrhages are common among patients with
bleeding/clotting disorders or those who are on anti coagulants.
DEFINITION
• Haemorrhage denotes the escape of blood from the cardiovascular
system to the surface of body or into its tissues or cavities.
CLASSIFICATION
1.Based on type of blood vessel involved
a. Arterial Haemorrhage
b. Venous Haemorrhage
c. Capillary haemorrhage
2.Based on time of occurrence
a. Primary Haemorrhage
b. Secondary Haemorrhage
c. Reactionary Haemorrhage
3.Based on visualization
a. External Bleeding
b. Internal Bleeding
4.Based on volume of blood loss
a. Mild Haemorrhage
b. Moderate Haemorrhage
c. Severe Haemorrhage
5.Based on speed of blood loss
a. Acute Haemorrhage
b. Chronic Haemorrhage
6.Based on percentage of blood loss
a. Class 1
b. Class 2
c. Class 3
d. Class 4
Primary Haemorrhage
• Occurs at the time of injury
• Body attempt to stop the bleeding by clot formation.
Secondary Haemorrhage
• Primary bleeding has stopped and wound start to bleed again after 24
hours and may continue for days.
• It may occur due to:
 Dislodgement of clot
 Secondary trauma to the wound
 Infections
Reactionary Haemorrhage
• Reactionary bleeding occurs within 8 hours after stoppage of primary
bleeding
• Caused due to loose foreign bodies in the wound like calculus,broken
bone piece,dislodgement of clot.
• Internal Haemorrhage
Bleeding that is confined within the body cavity and is not apparent on
the surface. Eg: Intra cranial bleeding
• External Haemorrhage
Blood escaping through a wound in the skin or mucosa.
Eg: Epistaxis
• Trauma
• Infection
• Local irritants
• Congenital malformations
• Surgical
• Haemophilia
• Liver disease
• Urinary infection
• Systemic diseases
• Abnormalities in clotting factors [eg :Haemophilia A]
• Abnormalities in platelets [eg :ITP]
CAUSES OF HAEMORRHAGE
• Increased pulse rate
• Increased pallor
• Restlessness
• Air hunger
• Thirst
• Cold clammy skin
• Tinnitus "ringing in the ears"
• Blindness
• Reduced urinary output
CLINICAL FEATURES
HAEMATOLOGICAL INVESTIGATIONS
Majority of defects of hemostasis can be screened by these
basic tests:
• Bleeding time
• Platelet count
• Prothrombin time
• Partial thromboplastin time
• Thrombin time
HAEMOSTASIS
Mechanism of cessation of extravasation of blood.
Four Important Phases Of Haemostasis
• Vascular phase : Injured vessels undergo constriction
• Platelet phase : Activation and platelet plug formation
• Coagulation phase : Activation of clotting,clot formation
• Fibrous organization or retraction of clot
STAGES OF HAEMOSTASIS
• Stage 1- Vasoconstriction
• Stage 2- Platelet plug
• Stage 3- Blood clot
Vasoconstriction
• Damage to the blood vessel causes narrowing of the lumen to limit the
blood loss.
• Local factors involved :
 Thromboxane A2
 Serotonin
 Fibrinopeptide B
Platelet plug formation
Platelet activation
• releases local factor,ADP ,thromboxane a2 causes more adhesion of
platelets.
Platelet adherence
• Von willebrand factor,integrins causes adherence of platelets to the
epithelial cells of blood vessels.
Platelet aggregation
• Caused by self association of platelets
Prothrombin Activation
• Prothrombin Thrombin
• Fibinogen Fibrin
Clotting Factors
• Factor 1 Fibrinogen
• Factor 2 Prothrombin
• Factor 3 Tissue Thromboplastin
• Factor 4 Calcium Ions
• Factor 5 Labile factor/Proaccelerin
• Factor 6 Unassigned
• Factor 7 Stable factor/Proconvertin
• Factor 8 Antihemophilic Factor
• Factor 9 Christmas Factor
• Factor 10 Stuart Power Factor
• Factor 11 Plasma Thromboplastin Antecedent
• Factor 12 Hageman Factor
• Factor 13 Fibrin Stabilizing Factor
Methods Of Achieving Haemostasis
1.Mechanical methods
• Pressure
• Hemostat
• Suture and ligation
2.Chemical methods
• Adrenaline
• Thrombin
• Surgicel
• Oxygel
• Gelatin sponge
• Microfibrillar collagen
• Fibrous glue
• Styptics and astringents
• Alginic acid
• Natural collagen sponge
• Fibrin sponge
• Bone wax
• Ostene
3.Thermal Agents
• Cautery
• Electro cautery
• Cryosurgery
• Laser
Management Of Secondary Haemorrhage In
Normal Patients
• This management occurs a few days after surgery,it involves the removal of
any debris from the wound surface.
• Identify the source of bleeding and treat as would be done in a patient with
secondary bleeding.
• Surgical stents can be placed over sockets for stabilization of clot and
prevention of wound contamination.
Management Of Haemorrhage In Patients With
Bleeding Disorders/Those On Anti Coagulant Therapy
• Pre-operative blood investigations should be carried out,pre-operative
correction of the underlying deficiency(replacement of clotting factors or
platelets).
• After this appropriate local measures to be carried out to decrease the
chances of post- operative bleeding.
Management Of Haemorrhage In Patients
With Uncontrolled Hypertension
• Prior appropriate medical consultation to decrease blood pressure.
• Once blood pressure is controlled,then bleeding decreases and with
local measures the hemorrhage is controlled.
WOUND HEALING
• Refers to the body's replacement of destroyed tissue by living tissues.
• Phases Of Wound Healing
1.Inflammatory Phase
2.Proliferative Phase
3.Re modelling Phase
Inflammatory Phase
• Begins when wound develops.
• Lasts 4 to 6 days immune system works to prevent microbial colonization.
• Marked by oedema,erythema,pain and inflammation.
Proliferative Phase
• Lasts another 4-24 days.
• Granulation tissue fills in the wound.
• Fibroblasts lay collagen in the wound bed.
• Wound edges begin to contract.
• Epithelial cells migrate from wound margins.
Re modelling Phase
• Lasts for several years.
• Collagenous matrix forms a scar after continuous remodelling.
• Stronger type 1 collagen replaces type 3.
• Any disruption during the phase leads to formation of exuberant scar
or wound dehiscence.
HEALING OF AN EXTRACTION SOCKET
• Healing by second intention.
• Blood fills extraction site after removal of tooth from socket.
• Both intrinsic and extrinsic pathways of clotting cascade are activated.
• Resultant fibrin meshwork containing entrapped RBCs seals off the torn
blood vessels and reduces the size of the extraction wound.
• Organization of clot begins within the first 24 to 48 hrs with dilation of blood
vessels,leucocyte migration and formation of a fibrin layer
• By 1st week
• The clot forms a temporary scaffold
• Epithelium at wound periphery grows over organizing clot.
• Stage of active crestal resorption.
• Angiogenesis in remnants of PDL ligaments.
By 2nd week
• Clot continues to get organized through fibroplasia.
• New blood vessels migrate to center of the clot.
By 3rd week
• Extraction socket filled by granulation tissue
• Surface of wound completely re epithelialized with minimal or no
scar formation.
COMPLICATIONS
• Hemorrhage
• Wound infection
• Abscess formation
• Cellulitis
• Necrosis or gangrene
• Keloid formation
• Delayed wound closure
RECENT ADVANCES
•Application and progress of inorganic composites in haemostasis: (April 2024)
This review focuses on the haemostatic mechanisms of silicate minerals (zeolite,
montmorillonite, and bioglass), silica (mesoporous silica and diatomaceous
silica), polyphosphates, inorganic carbon materials (graphene and carbon
nanotubes), metal-containing materials (metal–organic frameworks) and related
composite haemostatic materials.
 In recent years, inorganic composite haemostatic materials have received
widespread attention for their ability to rapidly stop bleeding and for their low
biotoxicity.
INORGANIC COMPOSITES A CALCIUM AND ZINC COMPOSITE ALGINATE
HYDROGEL
• A calcium and zinc composite alginate hydrogel for pre-operative hemostasis
& wound care-(2023 journal)
 Substantial in vitro efficacy
 Reduced bleeding time
 No evident hemolysis in human blood biodegradable
• The applications of polysaccharides in dentistry
(Frontiers in bioengineering and technology article-2022)
 Promising application in wound healing.
 Excellent biocompatibility,bio safety,anti inflammatory.
• A study named Assessment and comparison of the hemostatic efficacy
of ferrum phosphoricum against other conventional methods in minor
oral sugical procedures-International journal of applied dental
sciences(2021)
 Found that ferrum content helps balance iron & oxygen in
blood,phosphorous prevents bleeding.
 Shorten bleeding time,better healing.
• Topical and effective hemostatic medicines in the battlefield(2015)
 Uncontrolled hemorrhage has been considered as one of the most
important factors for causing death on the battlefront
 If given timely and efficient hemostatic medicines in pre-hospital setting,
patients will obtain more time and chance to wait for medical treatment so
as to save their lives.
 The hemostatic materials Hemcon and QickClot are widely used in the battle
and proved to be the most effective ways to stop bleeding. However, as new
agents get to emerge and the side effects of those well-known efficient
devices have been exposed gradually, people start to doubt the efficacy of
them. So Fibrin Sealant dressing, Celox and Woundstat are more effective
to stanch hemorrhage than others.
CONCLUSION
Control of haemorhage is the most important part of any surgical procedure.
The main step in prevention of hemorrhage in dental clinic is detailed history
taking of the patient,adequate precaution of apprehensive patient as
haemorrhages require medical attention and can be deadly.
REFERENCE
• Textbook of Oral and Maxillofacial Surgey by S M Balaji
• Textbook of Oral and Maxillofacial Surgery by Neelima Anil Mallik
• Peterson’s Principles of Oral and Maxillofacial Surgery
• International journal of applied dental sciences
thank you

HAEMORRHAGE power point presentationnnnn

  • 1.
  • 2.
    CONTENTS . Introduction . Definition .Classification . Causes Of Haemorrhage . Clinical Features . Hematological Features . Haemostasis . Stages Of Haemostasis . Methods Of Achieving Haemostasis . Wound Healing . Healing Of Extraction Socket . Complications . Recent Advances . Conclusion . Reference
  • 3.
    INTRODUCTION • Haemorrhage canoccur a greater or lesser degree during all surgical procedures. Major hemorrhages are common among patients with bleeding/clotting disorders or those who are on anti coagulants.
  • 4.
    DEFINITION • Haemorrhage denotesthe escape of blood from the cardiovascular system to the surface of body or into its tissues or cavities.
  • 5.
    CLASSIFICATION 1.Based on typeof blood vessel involved a. Arterial Haemorrhage b. Venous Haemorrhage c. Capillary haemorrhage 2.Based on time of occurrence a. Primary Haemorrhage b. Secondary Haemorrhage c. Reactionary Haemorrhage 3.Based on visualization a. External Bleeding b. Internal Bleeding
  • 6.
    4.Based on volumeof blood loss a. Mild Haemorrhage b. Moderate Haemorrhage c. Severe Haemorrhage 5.Based on speed of blood loss a. Acute Haemorrhage b. Chronic Haemorrhage 6.Based on percentage of blood loss a. Class 1 b. Class 2 c. Class 3 d. Class 4
  • 7.
    Primary Haemorrhage • Occursat the time of injury • Body attempt to stop the bleeding by clot formation. Secondary Haemorrhage • Primary bleeding has stopped and wound start to bleed again after 24 hours and may continue for days. • It may occur due to:  Dislodgement of clot  Secondary trauma to the wound  Infections
  • 8.
    Reactionary Haemorrhage • Reactionarybleeding occurs within 8 hours after stoppage of primary bleeding • Caused due to loose foreign bodies in the wound like calculus,broken bone piece,dislodgement of clot.
  • 9.
    • Internal Haemorrhage Bleedingthat is confined within the body cavity and is not apparent on the surface. Eg: Intra cranial bleeding • External Haemorrhage Blood escaping through a wound in the skin or mucosa. Eg: Epistaxis
  • 10.
    • Trauma • Infection •Local irritants • Congenital malformations • Surgical • Haemophilia • Liver disease • Urinary infection • Systemic diseases • Abnormalities in clotting factors [eg :Haemophilia A] • Abnormalities in platelets [eg :ITP] CAUSES OF HAEMORRHAGE
  • 11.
    • Increased pulserate • Increased pallor • Restlessness • Air hunger • Thirst • Cold clammy skin • Tinnitus "ringing in the ears" • Blindness • Reduced urinary output CLINICAL FEATURES
  • 12.
    HAEMATOLOGICAL INVESTIGATIONS Majority ofdefects of hemostasis can be screened by these basic tests: • Bleeding time • Platelet count • Prothrombin time • Partial thromboplastin time • Thrombin time
  • 13.
    HAEMOSTASIS Mechanism of cessationof extravasation of blood.
  • 14.
    Four Important PhasesOf Haemostasis • Vascular phase : Injured vessels undergo constriction • Platelet phase : Activation and platelet plug formation • Coagulation phase : Activation of clotting,clot formation • Fibrous organization or retraction of clot
  • 15.
    STAGES OF HAEMOSTASIS •Stage 1- Vasoconstriction • Stage 2- Platelet plug • Stage 3- Blood clot
  • 16.
    Vasoconstriction • Damage tothe blood vessel causes narrowing of the lumen to limit the blood loss. • Local factors involved :  Thromboxane A2  Serotonin  Fibrinopeptide B
  • 17.
    Platelet plug formation Plateletactivation • releases local factor,ADP ,thromboxane a2 causes more adhesion of platelets. Platelet adherence • Von willebrand factor,integrins causes adherence of platelets to the epithelial cells of blood vessels. Platelet aggregation • Caused by self association of platelets
  • 18.
    Prothrombin Activation • ProthrombinThrombin • Fibinogen Fibrin
  • 19.
    Clotting Factors • Factor1 Fibrinogen • Factor 2 Prothrombin • Factor 3 Tissue Thromboplastin • Factor 4 Calcium Ions • Factor 5 Labile factor/Proaccelerin • Factor 6 Unassigned • Factor 7 Stable factor/Proconvertin • Factor 8 Antihemophilic Factor • Factor 9 Christmas Factor • Factor 10 Stuart Power Factor • Factor 11 Plasma Thromboplastin Antecedent • Factor 12 Hageman Factor • Factor 13 Fibrin Stabilizing Factor
  • 20.
    Methods Of AchievingHaemostasis 1.Mechanical methods • Pressure • Hemostat • Suture and ligation 2.Chemical methods • Adrenaline • Thrombin • Surgicel • Oxygel • Gelatin sponge • Microfibrillar collagen • Fibrous glue • Styptics and astringents
  • 21.
    • Alginic acid •Natural collagen sponge • Fibrin sponge • Bone wax • Ostene 3.Thermal Agents • Cautery • Electro cautery • Cryosurgery • Laser
  • 22.
    Management Of SecondaryHaemorrhage In Normal Patients • This management occurs a few days after surgery,it involves the removal of any debris from the wound surface. • Identify the source of bleeding and treat as would be done in a patient with secondary bleeding. • Surgical stents can be placed over sockets for stabilization of clot and prevention of wound contamination.
  • 23.
    Management Of HaemorrhageIn Patients With Bleeding Disorders/Those On Anti Coagulant Therapy • Pre-operative blood investigations should be carried out,pre-operative correction of the underlying deficiency(replacement of clotting factors or platelets). • After this appropriate local measures to be carried out to decrease the chances of post- operative bleeding.
  • 24.
    Management Of HaemorrhageIn Patients With Uncontrolled Hypertension • Prior appropriate medical consultation to decrease blood pressure. • Once blood pressure is controlled,then bleeding decreases and with local measures the hemorrhage is controlled.
  • 25.
    WOUND HEALING • Refersto the body's replacement of destroyed tissue by living tissues.
  • 26.
    • Phases OfWound Healing 1.Inflammatory Phase 2.Proliferative Phase 3.Re modelling Phase
  • 27.
    Inflammatory Phase • Beginswhen wound develops. • Lasts 4 to 6 days immune system works to prevent microbial colonization. • Marked by oedema,erythema,pain and inflammation.
  • 28.
    Proliferative Phase • Lastsanother 4-24 days. • Granulation tissue fills in the wound. • Fibroblasts lay collagen in the wound bed. • Wound edges begin to contract. • Epithelial cells migrate from wound margins.
  • 29.
    Re modelling Phase •Lasts for several years. • Collagenous matrix forms a scar after continuous remodelling. • Stronger type 1 collagen replaces type 3. • Any disruption during the phase leads to formation of exuberant scar or wound dehiscence.
  • 30.
    HEALING OF ANEXTRACTION SOCKET • Healing by second intention. • Blood fills extraction site after removal of tooth from socket. • Both intrinsic and extrinsic pathways of clotting cascade are activated. • Resultant fibrin meshwork containing entrapped RBCs seals off the torn blood vessels and reduces the size of the extraction wound. • Organization of clot begins within the first 24 to 48 hrs with dilation of blood vessels,leucocyte migration and formation of a fibrin layer
  • 31.
    • By 1stweek • The clot forms a temporary scaffold • Epithelium at wound periphery grows over organizing clot. • Stage of active crestal resorption. • Angiogenesis in remnants of PDL ligaments.
  • 32.
    By 2nd week •Clot continues to get organized through fibroplasia. • New blood vessels migrate to center of the clot. By 3rd week • Extraction socket filled by granulation tissue • Surface of wound completely re epithelialized with minimal or no scar formation.
  • 33.
    COMPLICATIONS • Hemorrhage • Woundinfection • Abscess formation • Cellulitis • Necrosis or gangrene • Keloid formation • Delayed wound closure
  • 34.
    RECENT ADVANCES •Application andprogress of inorganic composites in haemostasis: (April 2024) This review focuses on the haemostatic mechanisms of silicate minerals (zeolite, montmorillonite, and bioglass), silica (mesoporous silica and diatomaceous silica), polyphosphates, inorganic carbon materials (graphene and carbon nanotubes), metal-containing materials (metal–organic frameworks) and related composite haemostatic materials.  In recent years, inorganic composite haemostatic materials have received widespread attention for their ability to rapidly stop bleeding and for their low biotoxicity.
  • 35.
    INORGANIC COMPOSITES ACALCIUM AND ZINC COMPOSITE ALGINATE HYDROGEL
  • 36.
    • A calciumand zinc composite alginate hydrogel for pre-operative hemostasis & wound care-(2023 journal)  Substantial in vitro efficacy  Reduced bleeding time  No evident hemolysis in human blood biodegradable • The applications of polysaccharides in dentistry (Frontiers in bioengineering and technology article-2022)  Promising application in wound healing.  Excellent biocompatibility,bio safety,anti inflammatory.
  • 37.
    • A studynamed Assessment and comparison of the hemostatic efficacy of ferrum phosphoricum against other conventional methods in minor oral sugical procedures-International journal of applied dental sciences(2021)  Found that ferrum content helps balance iron & oxygen in blood,phosphorous prevents bleeding.  Shorten bleeding time,better healing.
  • 38.
    • Topical andeffective hemostatic medicines in the battlefield(2015)  Uncontrolled hemorrhage has been considered as one of the most important factors for causing death on the battlefront  If given timely and efficient hemostatic medicines in pre-hospital setting, patients will obtain more time and chance to wait for medical treatment so as to save their lives.  The hemostatic materials Hemcon and QickClot are widely used in the battle and proved to be the most effective ways to stop bleeding. However, as new agents get to emerge and the side effects of those well-known efficient devices have been exposed gradually, people start to doubt the efficacy of them. So Fibrin Sealant dressing, Celox and Woundstat are more effective to stanch hemorrhage than others.
  • 40.
    CONCLUSION Control of haemorhageis the most important part of any surgical procedure. The main step in prevention of hemorrhage in dental clinic is detailed history taking of the patient,adequate precaution of apprehensive patient as haemorrhages require medical attention and can be deadly.
  • 41.
    REFERENCE • Textbook ofOral and Maxillofacial Surgey by S M Balaji • Textbook of Oral and Maxillofacial Surgery by Neelima Anil Mallik • Peterson’s Principles of Oral and Maxillofacial Surgery • International journal of applied dental sciences
  • 42.

Editor's Notes

  • #10 Idiopathic thrombocytopenic purpura Also called: ITP, immune thrombocytopenic purpura caused due to low platelet count
  • #11 pallor: paler than normal air hunger: need for air clammy skin; wet from sweating
  • #15 ADP : Adenosine diphosphate PAF : platelet activating factor
  • #31 Angiogenesis is the process of new blood vessels forming from existing blood vessels in the body